ACTH (1-17) TFA, an adrenocorticotropin analogue, is a potent human melanocortin 1 (MC1) receptor agonist with a Ki of 0.21 nM. Ki: 0.21 nM (human MC1 receptor)[1]
ACTH (1-17) TFA is a potent agonist at the hMC1R. ACTH (1-17) shows high affinity for the hMC1R with a Ki value of 0.21±0.03 nM which is slightly higher than that of 0.13±0.005 nM for alpha-MSH[1]. ACTH (1-17) induces a slight and not significant increase in growth hormone secretion even when micromolar concentrations of the peptide are employed in rat pituitary cultures[2].
Inhibition of DNA labeling is noted when the ACTH (1-17) is administered at 2 hr after the beginning of the daily dark span when nocturnal animals become active. When administered at this circadian stage, the larger dose in particular is associated with an inhibition of DNA labeling lasting for 24 hr. The inhibitory effect is much shorter when the same dose is injected 4 hr earlier[3].
[1]. Tsatmali M et al. ACTH1-17 is a more potent agonist at the human MC1 receptor than alpha-MSH. Cell Mol Biol (Noisy-le-grand). 1999 Nov;45(7):1029-34. [2]. Ceda GP, et al. The effects of ACTH (1-17) on GH secretion in vitro. Horm Metab Res. 1987 Aug;19(8):361-3. [3]. Walker WV, et al. Effect of an adrenocorticotropin analogue, ACTH (1-17), on DNA synthesis in murine metaphyseal bone. Biochem Pharmacol. 1985 Apr 15;34(8):1191-6.